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Reviews and Overviews
Cognitive Behavior Therapy for Depression?
Choose Horses for Courses
Gordon Parker, D.Sc., M.D.,
Ph.D., F.R.A.N.Z.C.P.
Kay Roy, B.A.
Kerrie Eyers, M.A., M.P.H.,
M.A.P.S.
Objective: Although cognitive behavior
therapy is a widely accepted treatment for
depression, the problematic nature of efficacy studies is insufficiently recognized.
within its theoretical underpinning, and
argued against viewing cognitive behavior therapy as a universal rather than a
targeted strategy.
Method: The authors reviewed original
studies and quantitative analyses on the
use of cognitive behavior therapy for
depression.
Conclusions: Although cognitive behavior therapy may act more by its nonspecific therapeutic ingredients, the authors
argued that by testing cognitive behavior
therapy’s efficacy in heterogeneous study
groups, rather than in specific subgroups,
failure to differentiate it from control
therapies may have been ensured.
Results: The authors suggeste d that
claims for cognitive behavior therapy’s efficacy on depression have been overstated, questioned whether its efficacy fits
(Am J Psychiatry 2003; 160:825–834)
Cognitive therapy is the most extensively researched
psychological treatment for nonpsychotic unipolar
outpatient depressive disorders (1).
C
ognitive behavior therapy evolved from cognitive
therapy, which focused on dysfunctional beliefs, and then
incorporated components of behavior therapy. Its role in
depression was detailed in a key treatment manual (2)
more than two decades ago.
While we observe clear benefit in many of our patients
receiving cognitive behavior therapy, a careful review of
the literature challenges cognitive behavior therapy as any
more efficacious than other nonpharmacological therapies. There is a need to progress beyond the methods used
so far to investigate cognitive behavior therapy’s efficacy.
In Western countries, antidepressant drugs and cognitive
behavior therapy dominate the treatment of depression.
Each has been tested in heterogeneous groups of depressed patients and, in direct comparisons, has been
found to have comparable overall efficacy. Studying heterogeneous groups is only appropriate, however, when a
treatment is effective for all expressions of depression. In
our view, studies have failed to identify the situations and
patient characteristics associated with effective cognitive
behavior therapy.
Clinical management of the depressive disorders currently risks the “affective fallacy”—in literature, a term
used to describe the error of evaluating a work by its effects on the reader rather than by the integral strengths of
the work itself. Similarly, the choice between antidepressant and cognitive behavior therapy for an individual paAm J Psychiatry 160:5, May 2003
tient often rests simply on the professional and personal
biases of the patient and therapist.
The Acute Phase of Depression
It is difficult to compare individual controlled studies of
cognitive behavior therapy because of methodological
problems associated with a psychotherapy that is variably
defined and administered. Assessment of response is also
problematic. For example, improvements associated with
cognitive behavior therapy have been claimed to occur
early in therapy (3), at mid-term (4), and after a significant
delay (5), raising questions about the appropriate endpoint for analysis and exacerbating the usual limitations
of meta-analysis. Although the treatment efficacy of cognitive behavior therapy in the acute phase of depression
has been evaluated in numerous reviews (e.g., references 1
and 6) and meta-analyses (e.g., references 7–10), an inconsistency across reports is worthy of emphasis.
Dobson (7) concluded that cognitive behavior therapy
was more effective than behavior therapy, other psychotherapies, and pharmacotherapy. The largest meta-analysis, by Gloaguen and colleagues (9), evaluated 48 randomized controlled trials that included 2,765 patients with
nonpsychotic and nonbipolar major depression or dysthymia. The treatment of patients receiving cognitive behavior therapy was quantified as superior to the “treatment” of an amalgamated group of wait-listed or placebocontrol subjects (20 studies, 29% improvement) and the
treatment of patients receiving antidepressant medication
(17 studies, 15% improvement) and “other therapies,”
such as supportive and nondirective psychotherapies, interpersonal psychotherapy, and relaxation therapy (22
studies, 10% improvement). Cognitive behavior therapy
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COGNITIVE BEHAVIOR THERAPY FOR DEPRESSION
was no better than behavior therapy (13 trials, 2% benefit).
The authors concluded that cognitive behavior therapy
had superior efficacy to both no therapy and all other modalities apart from behavior therapy.
Methodological concerns about this meta-analysis included the amalgamation of placebo-control and waitlisted patients into a composite group, therefore disallowing direct comparison with placebo “treatment.” A placebo, by definition, should “please,” while allocation to a
waiting list should discourage any improvement since the
therapeutic “gun” has yet to be “fired.” Comparison against
each group individually is required to understand cognitive behavior therapy’s efficacy. Their amalgamated analysis resulted in only one study with a placebo cell—the National Institute of Mental Health (NIMH) Treatment of
Depression Collaborative Research Program study by Elkin and colleagues (11). In fact, that cell was described by
the original authors as involving “placebo plus clinical
management,” with the latter component serving “as a
control for regular contact with an experienced and supportive therapist…[and thus] as a useful comparison
group for evaluating the specific effectiveness of the psychotherapies” (p. 977). The outcome there did not differ
significantly from the three active comparison treatments.
Thus, the influential meta-analysis by Gloaguen et al. (9)
did not truly compare cognitive behavior therapy to placebo, partially disallowing their conclusion that the effects
of cognitive behavior therapy “are not due to placebo and/
or demand characteristics.”
Second, their definition of the “other therapies” comparator group included multiple psychotherapies (as well
as relaxation therapy and alternative bibliotherapy), risking the less powerful therapies in this group, obscuring the
advantages of more efficacious psychotherapies, and thus
risking overstating cognitive behavior therapy’s efficacy.
Third, their conclusions are inconsistent with the earlier
Depression Guideline Panel meta-analysis (8), which considered 28 randomized controlled trials of psychotherapy
for depression. Response rates were 50% for cognitive behavior therapy, 52% for interpersonal psychotherapy, and
55% for behavior therapy; this equivalence is in contrast to
the conclusions reached in the study by Dobson (7) and
the meta-analysis by Gloaguen et al. (9). The latter studies
are also inconsistent with a meta-analysis by Leichsenring
(10) comparing the short-term efficacy of at least 13 sessions of cognitive behavior therapy and behavior therapy
with short-term psychotherapy and finding no difference
in effects on depressive symptoms, general psychiatric
symptoms, social functioning, or remission and improver
rates.
The meta-analyses suggested a narrower question: is
cognitive behavior therapy any more effective than nonspecific psychotherapy? Stravynski and Greenberg (12)
suggested that all models of psychotherapy, including cognitive behavior therapy, may be “equally unsound scientifically but they energize the therapists and provide useful
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fictions to activate the patients to lead somewhat more
satisfactory lives.” Ilardi and Craighead (3) suggested that,
since most symptomatic improvement with cognitive behavior therapy occurs before the formal introduction of
cognitive restructuring techniques, improvement reflects
more nonspecific treatment factors than the effects of specific cognitive behavior therapy. King (13) reviewed NIMH
study data (11) and comparisons between cognitive behavior therapy and 1) interpersonal psychotherapy, 2)
brief psychodynamic therapy, and 3) social work counseling and concluded that there was “no evidence that cognitive behavior therapy had superior short-term efficacy
compared to other psychological treatment, or indeed to
placebo.”
Despite such concerns, a conservative interpretation
suggests that cognitive behavior therapy is efficacious because it is superior to no treatment or the wait list control
condition. In terms of superiority to other manualized
psychotherapies or to basic clinical management, we suggest that the verdict of the efficacy of cognitive behavior
therapy as not proven holds (the Scottish judicial system
has an option of “not proven” as opposed to “guilty” or
“not guilty,” which is a useful call in this instance). Its efficacy may reflect nonspecific ingredients common to any
psychotherapy.
Ongoing Treatment
There are few continuation or maintenance studies of
cognitive behavior therapy. One (14) enrolled patients
with major depression in 16 weeks of acute treatment, followed by 2 years of maintenance. Group members received either antidepressant drugs or cognitive behavior
therapy for the acute and maintenance phases or antidepressants in the acute phase, followed by cognitive behavior therapy in the maintenance phase. There were no significant differences between treatments in improvement
or rates of relapse.
Most long-term studies have relied on naturalistic follow-up of patients in short-term comparison studies in
which treatment often ceased after the acute phase or
continued at varying levels of frequency and compliance
and used varying markers of outcome. The Depression
Guideline Panel review (8) suggested that the prophylactic
effects of acute-phase cognitive behavior therapy appeared superior to that of pharmacotherapy, although the
nature of the data (that is, from open studies) disallowed
definitive conclusions.
In the large meta-analysis by Gloaguen et al. (9), eight of
the 48 studies were judged as allowing a comparison of
cognitive behavior therapy with antidepressants at a follow-up point of at least 1 year, with respective rates of relapse of 29% and 60%. Five of those eight studies were also
included in an analysis by Scott (1), who noted that the
naturalistic follow-ups made comparison difficult but
concluded that there was a “trend for cognitive therapy
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PARKER, ROY, AND EYERS
(alone or in combination) to be nonsignificantly better
than maintenance pharmacotherapy in preventing relapse.” The more cautious tone of Scott was appropriate
when there was a mean cell size of only 13 subjects, while
the 1-year rates of relapse associated with antidepressants
in each articles’ analyses (60% and 65%, respectively) were
uncharacteristically high.
There is some indirect evidence of a prophylactic effect
of cognitive behavior therapy. Fava and colleagues (15, 16)
studied 40 patients with major depression, who, after tapering antidepressant therapy, were randomly assigned to
either cognitive behavior therapy for residual symptoms
or standard clinical management. The small study group
and the fact that some subjects required antidepressants
for relapse limited the study’s conclusions. Nevertheless,
lower rates of relapse were demonstrated for cognitive behavior therapy after 2, 4, and 6 years (25% versus 80%, 35%
versus 70%, and 50% versus 75%, respectively).
An important question is whether cognitive behavior
therapy has prophylactic potential in preventing relapse
or recurrence in partial responders to initial therapy, when
such subjects are at a greater risk of depression relapse
(17). Paykel et al. (18) and Scott et al. (19) investigated patients whose depression had partially remitted with medication and who were randomly assigned to clinical management alone or in combination with 20 weeks of
cognitive behavior therapy while continuing to take antidepressants. Medication and clinical management sessions were maintained during a 48-week follow-up phase.
There were no significant group differences over the 20week acute phase; formalized relapse rates tended to be
lower in the group receiving cognitive behavior therapy
(18), both at the end of the 20-week treatment phase (10%
versus 18%) and at the 68-week endpoint (29% versus
47%). Monthly depression scores showed an almost immediate improvement in the group receiving cognitive behavior therapy in self-report scores on the Beck Depression Inventory but not until the third month for blind,
observer-rated scores on the Hamilton Depression Rating
Scale. The rapid subjective effect of cognitive behavior
therapy suggests either a placebo effect (with subjects
aware of allocation to additional therapy) or a real cognitive impact after initial exposition and implementation of
cognitive behavior therapy.
Thus, some studies indicate ongoing benefits of cognitive behavior therapy, but they have generally compared
cognitive behavior therapy to treatment as usual or varying ongoing antidepressant therapies. The comparative
effectiveness of cognitive behavior therapy and medication is of fundamental importance to clinicians and patients, but the question has been confused by comparing
prophylactic cognitive behavior therapy with maintenance
medication treatment. It would be more appropriate to
compare cognitive behavior therapy’s prophylactic potential with cogent clinical management, nonspecific psychotherapy, and even psychodynamic psychotherapy
Am J Psychiatry 160:5, May 2003
(where the last has been held to demonstrate posttreatment improvement [20]) to determine if cognitive behavior therapy has specificity.
Superior to Other Psychotherapies?
As discussed, there is no clear consensus whether cognitive behavior therapy is superior or inferior to other psychotherapies, but there may be specific circumstances in
which cognitive behavior therapy offers advantages. For
example, Thase (21) suggested that the structured and directed components of cognitive behavior therapy are
more beneficial than introspective psychotherapy, in
which reflection on negative cognitions may overwhelm
severely depressed individuals. However, Scott (1) reviewed numerous studies examining predictors of response to cognitive behavior therapy and concluded that
research attempts “to characterize cognitive therapy responders have been disappointing.”
An important advantage to cognitive behavior therapy
might be in treating depression in patients with personality disorder, who are recognized as responding less well to
all forms of therapy (22). Some reports support special
benefits of cognitive behavior therapy (e.g., reference 23),
but most have been negative (e.g., references 24 and 25).
In regard to personality style, cognitive behavior therapy
has been shown to be more effective than interpersonal
psychotherapy for depressed patients with elevated levels
of avoidant personality (26) in the NIMH Treatment of Depression Collaborative Research Program study, which is
reassuring when such a style is an accepted risk factor for
depression.
Other NIMH analyses, as well as other studies (e.g., reference 27), have identified depressed patients with less cognitive dysfunction or fewer dysfunctional attitudes having
a superior response to cognitive behavior therapy (28)—
which is somewhat paradoxical when cognitive behavior
therapy is designed to redress dysfunctional attitudes.
Cognitive behavior therapy’s psychotherapeutic efficacy
has been linked to therapist characteristics, including the
therapist’s capacity to structure the treatment (29) and, in
particular, to his or her empathy (30). Robinson and colleagues (31) have noted that the newer psychotherapies
are more effective when practiced by “true believers,”
whether reflecting nonspecific effects of the therapist or
therapist proficiency. Thus, there is no clear evidence
identifying when cognitive behavior therapy might be superior to other forms of psychotherapy.
Superior to Antidepressant Drugs?
There are several theoretical situations in which cognitive behavior therapy may be superior to antidepressant
medication, for example, when patients have antipathy to
medication, an inability to tolerate medication, or are at
special risk (e.g., pregnancy, high suicidality). Nonmedicahttp://ajp.psychiatryonline.org
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COGNITIVE BEHAVIOR THERAPY FOR DEPRESSION
tion options can be useful when there are concerns about
prescribing antidepressant drugs to children and adolescents—a group for whom cognitive behavior therapy is
said to be of benefit (32)—and, in particular, to prevent
recurrence (33).
Thase (21) and Fava et al. (34) observed that there were
many reports of patients with “drug-resistant” depressive
disorders responding to cognitive behavior therapy, so patients with nonresponsive and partially responsive disorders may benefit. The studies reported by Paykel et al. (18)
and Scott et al. (19) support such a role, while the report by
Fava et al. (34) found a 63% rate of remission in a course of
cognitive behavior therapy in patients who had achieved
no benefit in two antidepressant trials.
Augmentation of
Antidepressant Drugs?
Conte and colleagues (35) conducted a meta-analysis of
studies investigating psychotherapy and pharmacotherapy, separately and in combination, and concluded that
the combination was slightly more effective. Although several cognitive therapy and behavior therapy studies were
included in the overall analysis, neither was specifically
examined in the analyses of combination effects.
It has been claimed that combination therapy with
cognitive behavior therapy is particularly beneficial for
chronic and treatment-resistant depression (21, 36, 37) as
well as recurrent depression (38), but few such studies have
been reported. One (39) found some support in chronically
ill and severely depressed subjects, with combination therapy showing slight superiority to cognitive behavior therapy or pharmacotherapy alone. The most positive study (4)
suggested synergistic benefits in chronic depression, with
subjects receiving either nefazodone alone, cognitive behavior therapy alone, or the combination of the two; respective rates of remission were 29%, 33%, and 48%. The
study design requires repeating with antidepressant drugs
of broader action.
Paykel (40) noted that combination therapy could aid
medication compliance but, apart from some anecdotal
reports, was unable to find any systematic controlled trials
of any such effect. Thus, the empirical literature in regard
to cognitive behavior therapy is slight, and there is a need
to clarify whether any benefits emerge from the combination of medication and cognitive behavior therapy itself,
from varying sequences of medication and cognitive behavior therapy, or from effects on compliance.
Relation to the Cognitive Theory
of Depression?
Bowlby (41) argued that early attachment anomalies,
especially uncaring and/or overprotective parenting, generate cognitive schema or internal working models that
negatively shape the child’s later interpretation of inter-
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personal interactions, therefore inducing and maintaining
depression. Beck et al. (2) developed the model and advanced the application of cognitive behavior therapy, stating that his reformulation involved the depressed patient
having a “global negative view of himself, the outside
world, and the future” (the so-called cognitive triad), negative schemas (or stable faulty cognitive patterns), and
cognitive errors (or faulty information processing) (2). He
proposed that both stable depressogenic schema and situation-specific cognitive distortions contributed to depression (42). The first component is essentially a diathesis
stress construct; the second suggests that stressful events
reactivate earlier beliefs to precipitate depression.
If his model is valid, we would expect depressed individuals to show cognitive vulnerabilities upon recovery.
Our review of more than 30 studies (43) failed—almost
without exception—to identify differences between individuals with and without a history of depression. It is
possible that the measures used—most commonly the
Dysfunctional Attitudes Scale (44) and the Automatic
Thoughts Questionnaire (45)—may not truly measure
core beliefs and schemas. Ingram and colleagues (43) also
suggested that negative studies could be explained by the
enduring depressogenic schema existing at a deeper
level, while Miranda and colleagues (46) similarly argued
that cognitive vulnerability factors remain dormant,
awaiting activation by a negative mood. Thus, predisposed individuals may have latent beliefs awaiting activation by stress and only measurable under conditions of
stress. If so, their presence should be identifiable before
the first depressive episode. Our review with Gladstone
(47) identified only one supportive study (48).
Burns and Spangler (49) examined patients treated with
cognitive behavior therapy over a 1-week period. They
found no support for three hypotheses: 1) a cognitive mediation hypothesis—that changes in dysfunctional attitudes lead to changes in depression during treatment, 2) a
mood activation hypothesis—that changes in depression
lead to changes in dysfunctional attitudes, and 3) a circular causality hypothesis—that negative emotions and dysfunctional attitudes have reciprocal causal links. Their
analyses favored a common cause model, with a state depressogenic factor driving both depression and dysfunctional attitudes (e.g., a loss of hope) and with therapy providing hope. However, Teasdale (50), who argued for a
“shift in construct accessibility” model, showed that recovery associated with cognitive behavior therapy (in lieu
of pharmacotherapy) involves modifying emotional processing, therefore changing the capacity of triggering
clues to reactivate depressogenic processing.
Is it possible to define more homogeneous subsets of
individuals for whom the cognitive theory is relevant? Our
key-and-lock hypothesis (51, 52) views “locks” (cognitive
schemas laid down by early adverse events) as being
primed when an individual faces a mirroring life event (a
“key”). Key-lock links were found in only a minority of indiAm J Psychiatry 160:5, May 2003
PARKER, ROY, AND EYERS
viduals, were more common in nonmelancholic depression, and, seemingly counterintuitively, were more evident
in those with reactive rather than neurotic depression. We
suggested that reactive depression might be less a response
to a severe stressor and more a response to a mirroring
stressor that activates latent cognitive schema. Other analyses (e.g., reference 52) failed to find clear evidence that
cognitive schema were latent locks and favored them as
consequences of (or elicited by) a depressed mood. That is,
when depressed, an individual may feel worthless (or
hopeless) and then interpret recent stressors and the earlier environment according to the cognitive impact of the
depression, in line with the Teasdale model (50).
DSM-IV includes a category for depressive personality
disorder, with criteria including self-beliefs of inadequacy,
worthlessness, and low self-esteem. Individuals with such
symptoms appear ideal for assessing the relevance of cognitive behavior therapy, but we suspect a paradox. Since
many have experienced profound childhood privation, the
capacity of cognitive behavior therapy (like any other psychotherapy) to improve resilience may be limited. Resistance of such individuals to cognitive behavior therapy
may explain the apparently paradoxical results from the
NIMH Treatment of Depression Collaborative Research
Program study, in which those with more cognitive dysfunction (as shown by higher dysfunctional attitude
scores) benefited less from cognitive behavior therapy (28).
In summary, the theoretic basis for cognitive behavior
therapy in depression is difficult to validate. We suggest
that viewing cognitive behavior therapy as potentially effective across heterogeneous expressions of depression
leads to its being tested in those in whom a cognitive predisposition may be of quite variable relevance. A state influence model might apply in most instances and a diathesis stress model in only a minority.
Relation to Depression Severity?
It is uncertain whether cognitive behavior therapy is
equally efficacious in depression of varying severity. The
8-week NIMH Treatment of Depression Collaborative Research Program study (11) compared four treatments for
major depression: imipramine, cognitive behavior therapy, interpersonal psychotherapy, and placebo plus clinical management, each having comparable rates of response. However, in a subset of more severely ill patients,
imipramine was superior (53). There are several other
studies suggesting that severely depressed patients are unlikely to respond well to cognitive behavior therapy (e.g.,
references 54 and 55).
DeRubeis and colleagues (55) undertook a mega-analysis of four randomized trials and concluded that cognitive
behavior therapy “fared as well as antidepressant medication with severely depressed outpatients.” In response,
Klein (56) noted the “flawed nature of the cited data,” the
failure to consider relevant databases, and the “irreleAm J Psychiatry 160:5, May 2003
vance of placebo-free experimental designs to claims for
equivalent efficacy.” Others have accepted a differential
effect of cognitive behavior therapy across varying grades
of severity. Shapiro and colleagues (57) found that severely
depressed patients improved substantially more after 16
than after eight sessions. Thase and colleagues (58) proposed that the difference in improvement reflected a
slower response rate and recommended more intensive or
extended courses for more severely depressed patients.
We suspect that severity may sometimes serve as a
proxy for biological depressive conditions such as melancholia and that it may be more important to examine the
efficacy of cognitive behavior therapy across differing depressive disorders.
Is Efficacy Comparable
for All Depressive Subtypes?
The depressive disorders essentially comprise three
classes—psychotic, melancholic, and a heterogeneous
residue of nonmelancholic disorders. The first two classes
are generally viewed as more biological disorders, having a
low placebo response and superior responses to physical
treatments such as drugs and ECT. Their low rate of nonspecific improvement suggests that each is unlikely to respond to psychotherapy or to nonspecific elements of
therapy. Conversely, the high nonspecific improvement of
nonmelancholic depression means that any therapy has
considerable potential for nonspecific improvement.
There are no data specifically examining the efficacy of
cognitive behavior therapy in psychotic depression, suggesting its inappropriateness, while the situation for melancholia is more problematic. It is commonly claimed
(e.g., reference 59) that melancholia/endogenous depression is unresponsive to nonsomatic treatments, but early
studies of cognitive behavior therapy (e.g., references 39
and 60) reported a positive response. Thase and Friedman
(61) reported an uncontrolled study in which 38 patients
with Research Diagnostic Criteria-defined endogenous depression received 20 weeks of cognitive behavior therapy
sessions, and 70% responded. One report from the NIMH
study (28) concluded that “endogenous depression was an
overall predictor of lower depression severity at termination across all conditions,” but elsewhere it was stated that
the relationship “was not observed” for cognitive behavior
therapy. A key difficulty in analyzing such studies is that
melancholia is variably defined and diagnosed.
A review (61) noted such limitations before concluding
that the “data are somewhat suggestive that cognitive behavior therapy and behavior therapy are useful treatments
for some outpatients with endogenous depressive features” (p. 7) but that “there is still not yet compelling evidence that they (i.e., those with melancholia) will respond
as well to psychotherapy as pharmacotherapy” (p. 15).
We now consider the situation in regard to nonmelancholic depression. Most studies of patients with cognitive
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behavior therapy have been undertaken in patients with
diagnoses of major depression or dysthymia. Such diagnoses reflect a nominalistic approach to psychiatric nosology, with patients diagnosed as having, for example, major
depression more distinguished by the commonality of its
label than by the commonality of its essence.
In such a case, high placebo and spontaneous rates of
remission are observed, limiting the capacity to assess the
true efficacy of any treatment and best illustrated for major depression, in which the apparent equivalence of quite
different treatments is striking. For antidepressant drug
efficacy, a representative analysis by Janicak et al. (62)
quantified the rates of response as 63% to tricyclic antidepressants (in 79 studies), 66% to a monoxidase inhibitor
(in 16 studies), and 60% to 79% to four selective serotonin
reuptake inhibitors (in 21 studies). Comparisons of drug
treatments and psychotherapy suggest similar rates of response. For example, Robinson et al. (31) examined 60
psychotherapy studies and, although treatment outcome
for psychotherapy was somewhat superior to that of pharmacotherapy, only trivial differences were evident after
control for the researcher’s allegiance to psychotherapy.
Similar rates of response emerge across other treatment
modalities. For instance, Williams et al. (63) quantified a
62% rate of response (across 14 studies) to hypericum (St.
John’s wort), and Mynors-Wallis and Gath (64) reported
similar responses to problem solving and antidepressant
medication.
Such data suggest that about two-thirds of patients with
major (nonmelancholic) depression improve in response
to nonspecific factors. In representative trials (62), placebo rates of response ranged from 32% to 48%, while
Quitkin (65) suggested a placebo response rate in drug trials of 25% to 60%. Kirsch and Sapirstein (66) argued that
response during receipt of an antidepressant drug comprises 24% natural history, 51% placebo effect, and 25%
true drug effect. If similar response proportions apply to
other therapies, it may be impossible to demonstrate a differential effect of treatment in patients with nonmelancholic depression.
We suspect that cognitive behavior therapy is more efficacious for nonmelancholic depression than in other
types of depression but that efficacy estimates are influenced by the high responsiveness of those in the heterogeneous nonmelancholic group. It is unhelpful to continue
to study the efficacy of cognitive behavior therapy across
broad spectra (such as major depression and dysthymia)
and expect differentiation from other treatments. More information is required on the subgroups that do and do not
respond.
Application and Tolerability
Establishing the effectiveness of any psychosocial treatment is complicated by a range of variables in the therapy,
therapist, and patient that are less important in the evalu-
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ation of physical treatments. These include the varied
backgrounds, disciplines, and competence of therapists as
well as paradigm fidelity (67), particularly since the ability
to structure the treatment may be the component most
closely related to outcome (68).
Keijsers and colleagues (69) identified qualitative aspects of the therapeutic relationship that affect outcomes
of cognitive behavior therapy and suggested that cognitive
behavior therapy appears to require more active direction
by the therapist and higher levels of emotional support
than insight-oriented therapies. Characteristics of the
therapist associated with outcomes of superior cognitive
behavior therapy include standard nonspecific components (i.e., empathy, nonpossessive warmth, and positive
regard) as well as the patient perceiving the therapist as
self-confident, skillful, and active (70). Patients who rated
their therapist as significantly less empathic were more
likely to drop out of therapy, not complete homework assignments, and fail to improve (71).
In contrast to studies demonstrating the importance of
therapist characteristics, a randomized controlled study
found computer-assisted therapy, which allowed targets
for change to be chosen by the patient, to be as effective as
therapist-delivered cognitive behavior therapy (72).
Judging the effectiveness of any therapy includes consideration of tolerability and side effects. Jarrett et al. (73)
compared cognitive behavior therapy and treatment with
phenelzine in a 10-week trial for patients with atypical depression. The two active treatments demonstrated identical rates of response (58%), which were superior to that of
placebo (28%). However, attrition rates were 14% for cognitive behavior therapy, 25% for phenelzine, and 64% for
placebo, while adverse side effects were more likely to be
reported by those receiving phenelzine than those receiving placebo (92% versus 53%). Tolerability is likely to influence patients’ initial interest in pursuing any therapy and
subsequent compliance.
Possible Action
Cognitive behavior therapy may, as originally proposed,
modify ongoing cognitive vulnerabilities, effecting a specific antidepressant action. This may also exert a prophylactic effect, either directly or indirectly, by modifying risk
threshold and/or encouraging behavioral strategies that
redress dysfunctional cognitive attributions. If this is valid,
two issues must be reconciled. As noted earlier, the authors of the NIMH Treatment of Depression Collaborative
Research Program study observed (28) that “it appears
that the least cognitively impaired patients responded
more favorably to cognitive therapy,” challenging any effect of specific cognitive behavior therapy on underlying
cognitive dysfunction. More important, symptomatic improvement may occur in the course of cognitive behavior
therapy before cognitive restructuring (3). If initial improvement reflects the impact of hope and other nonspeAm J Psychiatry 160:5, May 2003
PARKER, ROY, AND EYERS
cific therapeutic ingredients, to what extent is the improvement trajectory further influenced by any specific
influence of cognitive behavior therapy?
Second, either the cognitive therapy or behavior therapy
component of cognitive behavior therapy may be central
and the other secondary. As stated earlier, several metaanalyses have suggested that cognitive behavior therapy is
no more effective than behavior therapy, although individual comparison studies (e.g., reference 68) have generally
failed to establish any differential outcome between, or
target impact of, cognitive behavior therapy and behavior
therapy. It is possible that the cognitive therapy component provides logic for a behavior therapy effect.
Third, nonspecific treatment and therapist effects (71)
are likely to make a significant contribution to any psychotherapy as far as good clinical management.
Fourth, the structure of cognitive behavior therapy may
provide an effective matrix for therapy. Scott (74) and Stravynski and Greenberg (12) identified common factors in
effective psychotherapy. They provided a new frame of reference and a clear rationale, identified a structure with
logical sequences and achievable goals, encouraged independent use of skills, changed the attributions of the patient, encouraged self-efficacy, and were active and directive. Cognitive behavior therapy clearly meets such
criteria, having logic and possessing a credibility that appeals both to patients and to therapists. Hardy and colleagues (75) suggested that cognitive behavior therapy has
a “treatment principle credibility” advantage that acts before the first treatment.
Fifth, cognitive behavior therapy invites patients to participate in the process of treatment and thus retain or regain control over their lives, which is important when
many depressed individuals lack mastery, either intrinsically or as a consequence of depression.
Sixth, cognitive behavior therapy meets many needs of
consumers not to merely receive a drug but rather to have
extended contact with a professional and sense made of
their personal world.
Seventh, cognitive behavior therapy may act on higherorder or antecedent constructs with any impact on depression being a secondary downstream component. Anxiety is a key candidate, as it increases the chance of depression and is responsive to cognitive behavior therapy.
However, there is no evidence that comorbid anxiety predicts a superior response to cognitive behavior therapy. In
fact, a majority of studies (e.g., reference 76) suggest the
opposite, although another report (77) has indicated that
those with high anxiety scores required more sessions of
psychotherapy.
Conclusions
Cognitive behavior therapy has long been accepted as a
credible therapy for depression. Despite high use and numerous evaluative studies, its efficacy (both acute phase
Am J Psychiatry 160:5, May 2003
and prophylactic) remains to be clarified, while proposed
mechanisms of action may not be consistent with cognitive theories of depression.
We offer two possible conclusions about the true status
of cognitive behavior therapy as a primary treatment for
depression. First, cognitive behavior therapy is of equivalent efficacy and utility as other psychotherapies or basic
clinical management, but it has a higher cachet because of
extensive scientific evaluation and its credibility to patients and practitioners as a rational and logical approach.
Second, cognitive behavior therapy is like all other antidepressant strategies, with gradients of benefit across heterogeneous groupings of disorders, such as major depression and nonmelancholic depression, and with the most
appropriate primary and secondary treatment niches yet
to be defined.
However, the efficacy and role of cognitive behavior
therapy will remain undefined if psychiatry continues to
accept the current dimensionally weighted model of depression, which uses pseudocategories to capture dimensional extremes and then argues that any therapy is equally
effective across a heterogeneous group. When therapies
are tested according to that model, all appear similarly efficacious. The message that “everyone’s a winner” then allows practitioners to back any horse in any race. Currently,
a practitioner’s discipline or interest (rather than characteristics of the depressive disorder and the patient) may
dictate which therapy is chosen—so demonstrating the affective fallacy.
We suggest that it is time to focus on determining the
circumstances in which cognitive behavior therapy might
be a specifically effective primary treatment. Until now,
evaluation has conformed to the scientific model of undertaking randomized and controlled trials of cognitive
behavior therapy as a primary universal treatment, revealing little definitive information about its specific efficacy
and effectiveness. It is not useful to ask whether surgery or
chemotherapy is a superior universal treatment for breast
cancer. Each, depending on the circumstances, may be
more effective and have advantages as a primary treatment, and neither excludes the use of the other or additional approaches. Furthermore, cancers are not classified
as belonging to severity-based heterogeneous groups
(e.g., major cancer, minor cancer, or subclinical cancer).
Decisions about cancer treatment respect etiology, disease classification, and subsequent empirical testing of
specific-treatment modalities.
Stravynski and Greenberg (12) argued for the need for
more pragmatic distinctions (e.g., medication for those
whose neurotransmission is disturbed, marital therapy for
those with marital difficulties, cognitive behavior therapy
for those with irrational thinking, and social skills for
those with interpersonal difficulties). However, such a
model still fails to address the possible advantages of sequencing different treatments or the use of primary and
adjunctive therapies. It has been said that “search[ing] for
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COGNITIVE BEHAVIOR THERAPY FOR DEPRESSION
subgroups of patients who may preferentially respond to
cognitive behavior therapy or pharmacotherapy has not
been fruitful” (7), but most attempts have been exploratory, involved retrospective analyses of data sets assembled for disparate reasons, and examined depressive subtype influences in limited ways.
Further exploration of subgroups responsive to cognitive behavior therapy as a primary therapy could involve
studying patients who appear to have achieved not just
acute or sustained benefit but also greater resilience to future episodes. This may define characteristics such as clinical features, illness patterns, temperament and personality, cognitive style, attitudes toward therapy, and
willingness to address behavioral tasks. In preparing this
article, we found reasonable consistency when asking
therapists to provide a prototypical true responder to cognitive behavior therapy. Responders were more commonly
women with good general coping skills who were committed to their work and to others, with that commitment
seemingly covering poor self-esteem or perceived limitations that were making them vulnerable to depression in
certain circumstances. They found the theory of cognitive
behavior therapy sensible and intellectually appealing, related well to the therapist, and actively engaged in the exercises to promote behavioral change. If true responders
can be profiled, then controlled studies could test the effectiveness of cognitive behavior therapy in progressively
extended subgroups to determine the limitations of therapy. It would be useful to engage in a similar process to
identify responsiveness to cognitive behavior therapy as
an adjunctive strategy.
If similar approaches were undertaken to evaluate other
antidepressant modalities (and, for antidepressant drugs,
specific drug classes), we might progressively develop a
more rational treatment matrix whereby depressed individuals would be provided with sequenced treatment options appropriate to the characteristics of their disorders.
The current treatment model for depression lacks “horse
sense” in encouraging the view that any therapeutic modality should be universal rather than targeted. It is likely
that cognitive behavior therapy (like other treatments) has
specific benefits both as a primary treatment and as an adjunctive treatment for certain subsets of depressed patients. For those who wish to back the cognitive behavior
therapy “horse,” it would be better to first define its form.
Received Feb. 12, 2002; revision received Aug. 6, 2002; accepted
Oct. 12, 2002. From the School of Psychiatry, University of New South
Wales, Sydney, N.S.W., Australia; and the Black Dog Institute, Prince
of Wales Hospital. Address reprint requests to Dr. Parker, Euroa Unit,
Prince of Wales Hospital, Randwick 2031, Sydney, N.S.W., Australia;
[email protected] (e-mail).
Supported by a program grant from the Australian National Health
and Medical Research Council (993208).
The authors thank their colleagues in the Mood Disorders Unit
and Heather Brotchie and Tony James for assistance with article
preparation.
832
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